Hormone Location stimulation inhibition Mode of action effects Times of

secretion
Corticotr Paraventric Stress -secreted into the primary capillary plexus of
opin ular nuclei the hypophyseal portal system in the
releasing of median eminence of the hypothalamus
hormone hypothala
mus
ACTH -anterior CRH -ACTH binds to receptor; g protein alpha -steriodogenesis
pituitary subunit activates adenylyl cyclase
increase levels of cAMP

-cAMP activates protein kinase

-protein kinase activates cholesteryl ester

hydrolase which converts cholesteryl esters
(from LDL) into cholesterol

-cAMP also activates steroidogenic acute

regulatory protein which mediates the
transport of newly liberated cholesterol into
the mitochondria

-in the mitochondria and ER cholesterol is

converted into the steroid hormones
Cortisol Adrenal -ACTH (produced -in circulation, cortisolis bound to CBG -↓ CRH, and ADH -high in
cortex: from cleavage of early
zona POMC) -disassociates from protein and diffuses -↑ in appetite morning
fasciculate across cell membrane
-stress -maintain sensitivity to vasoconstrictors -low in
and zona
-binds to cytoplasmic receptor causing late
reticularis - ↑ gluconeogenesis in liver
receptor disassociation from HSP70, HSP90, evening
and IP
-fetal lung development
-when
-horome-receptor complex diffuses into change
-↓ACTH
nucleus and activates or inhibits sleeping
transcription -↑GFR habits,
the cycle
-time delay because mechanism of action -↑ bone reabsorption
changes
affects transcription
-↓ insulin sensitivity

-immune system suppression

-↓collagen synthesis

Muscles

↑ protein degradation

↓protein synthesis

↓glucose utilization

↓sensitivity to insulin

Liver

↑glycogen storage

↑gluconeo by ↑ activity and amount of

enzymes

Fat

↓glucose utilization

↓sensitivity to insulin

↑lipolysis (oxidation of fatty acids)

 ↑ fat mobilization which ↑ their utilization
for energy

GHRH Ventomedi GH -binds to receptor activating adenylyl

al nucleus cyclase causing an increase in cAMP which
of glucocorticoi increases transcription to make new GH and
hypothala ds causes an influx of Ca to cause fusion of GH
mus secretory vesicle with membrane
GH Anterior -amino acids -glucose -causes growth of almost all tissues -pulsatile
pituitary pattern
-starvation -GH -promotes increased size of cell and
increased mitosis with devo of greater
-hypoglycemia -IGF-1 number of cells
-exercise -cortisol Adipose tissue
-stage ¾ sleep -somatostati ↓glucose uptake
n
-gonadal ↑lypolysis
steroids/thyroid
hormone ↓adiposity

Fat used instead of carbs for E

 Liver

↑gluconeogenesis

↑IGF-1

Muscle

↓glucose uptake

↑amino acid uptake

↑protein synthesis

↑lean body mass

↓catabolism of proteins

IGF-1 liver GH Muscle

↓glucose uptake

↑amino acid uptake

↑protein synthesis

↑lean body mass

↓catabolism of proteins

Bone, heart, lung

↑protein synthesis

↑DNA, RNA expression

↑cell size/number

↑organ size

↑organ function
 Chondrocytes

↑amino acid uptake

↑ protein synthesis

↑ DNA, RNA expression

↑collagen

↑chondroitin sulfate

↑cell size/number

↑linear growth

somatost hypothala IGF-1 -inhibits release of GH from pituitary

atin mus
glucocorticoids
TRH Hypothala Stimulates release of TSH from pituitary
mus
-activates phospholipase second messenger
system in pituitary to produce large amounts
of phospholipase C, Ca2+, and DAG leading
to TSH release
TSH Pituitary TRH thyroid 1. TSH stimulates iodide pump on basal -causes proliferation of thyroid gland
hormone membrane of follicular cell resulting in iodide
trapping ↑ proteolysis of thyroglobulin stored in
follicles
2. peroxidase on apical membrane oxidizes
iodide to iodine so it can readily bind to ↑ activity of iodide pump
tyrosine of thyroglobulin in the colloid
↑iodination of tyrosine t form thyroid
3.ER and golgi synthesize and secrete hormone
thyroglobulin
↑size and activity of thyroid cells
4.in colloid, iodine binds with the aid of
↑number of thyroid cells and change from
iodinase to tyrosine residues of
cuboidal to columnar
thyroglobulin

5.T3 ad T4 are cleaved from thyroglobulin,

pinocytic vesicles grab chunks of colloids

6. lysosomes with proteases digest TG

releasing T3 and T4 that diffuse across the
base of the cell into capillaries

7. everything else is recycled back to the

 colloid

T4 and Thyroid TSH -circulates bound to proteins ↑cardiac output, tissue blood flow, HR,
T3 gland respiration, contractility
-T3 binds thyroxine binding globulin and
albumin

-T4 binds thyrozine binding globulin, ↑basal metabolic rate

albumin, and thyroxine pre-albumin
(transyrethin) ↑mitochondria (↑ rate of formation of ATP
to energize cellular function)
--slow onset and long duration of action
because tightly bound and acts through ↑Na/K ATPase (active transport of ions)
transcription and translation
↑O2 consumption

↑glucose absorption/uptake
-at target T3 and T4 diffuse across
↑gluconeogenesis
membrane
↑glycogenolysis
-T4 is deiodinated to T3 which is more
biologically active ↑lipolysis

-T3 diffuses into nucleus where it binds to ↑protein synthesis

receptor which is bound as a heterodimer to
retinoid X receptor

-hormone bound receptor binds to hormone ↑adrenergic responses (↑sensitivity to

response element sympathetic; beta receptor activity;
receptor numbers in
-results in increase or decrease in heart,liver,muscle,adipocytes, G alpha
transcription of genes expression)

-promote growth and devo of fetal brain

Insulin Beta cells Glucose somatostatin -synthesize as a preprohormone by RER and ↑glucose transport by ↑ GLUT4 receptors -during
of then cleaved in ER to form proinsulinand on membrane meals
pancreas Amino acids cleaved again in Golgi to form insulin and c
peptide ↑protein synthesis (more permeable to
Fatty acids amino acid)
GH/cortisol ↑fat synthesis and storage
(indirect) -insulin binds to receptor (4 subunits help
together by disulfide bonds) ↓gluconeogenesis in liver
GI hormones
(amplifier) -binding causes beta subunits to undergo ↑ glycogen storage (inactivates liver
phospholipase so no splitting of glycogen
 Fed state autophosphorylation which activates ↑glycolysis
tyrosine kinase
↑ growth and gene expression
-tyrosine kinase p-lates insulin receptor
substrates (intracellular enzymes)
Plasma

↓glucose

↓FFA

↓ketoacids

↓amino acids
Glucagon Alpha cells Amino acids Glucose -activates adenylyl cyclase in hepatic cell ↑blood glucose
of membrane
pancreas Acetycholine Insulin ↑ break down of glycogen
-increase in cAMP
Ep/NE Somatostatin ↑gluconeogenesis from a.a.
-activates protein kinase which leads to de
VIP Ketones p-lation and degradation of glycogen
releasing glucose
CCK FFA

Fasting state
Glucagon Gut Feeding ↑ insulin response to glucose; amplifier
like
peptide ↑beta cell mass
Leptin Released Increased fat -acts on hypothalamus ↑ satiety
from
adipocytes -causes ↓ production of NPY and AGRP ↓hunger

-activation of POMC and alpha MSH

-↑CRH to ↓ food intake

-↑sympathetic activity

-↓ insulin
Ghrelin Released fasting -acts within hypothalamus ↑hunger Peak just
from GI before
tract eating
and falls
after
meal
PTH Chief cells Low plasma Ca High plasma Ca binds to receptor which activates an -Ca and PO4 resorption from bone
of Ca inhibitory g protein that decreases activity of
parathyroi adenylyl cyclase and cAMP which decreases -↓Ca excretion from the kidneys
d PTH released
 ↑renal phosphate excretion that overrides
the resorption from bone

-stimulates formation of 1,25 OH2D3

GnRH Hypothala Progesterone -stimulates pituitary to release FSH and LH puslatile
mus
-possible
estrogen

-testosterone
LH Released -GnRH Follicular -use cAMP messenger system -stimulates ovulation of ripe follicles and -peak in
from phase formation of corpus luteum utero for
pituitary Midcycle -acts on Theca cells resulting in the oogonia
-estrogen production of androgens devo
-estrogen
-stimulates leydig cells to synthesize and -surge
secrete Testosterone prior to
Luteal
ovulation
Phase

Progesterone

-hCG

-testosterone
FSH Released -GnRH Follicular -uses cAMP messenger system -stimulates growth of follicle and estrogen -peak in
from phase in females utero for
pituitary Midcycle -acts on the granulose cells resulting in oogonia
-estrogen synthesis of pregnenolone which is give to devo
-estrogen theca cells and production of aromatse to
convert androgens that the theca produce to -acts on sertoli cells to promote maturation -peak 6
make estradiol and estrone of sperm months
Luteal
for final
Phase
sexual
Progesterone differenti
ation

-hCG

-inhibin
Estrogen Ovaries, FSH/LH -promotes proliferation and growth of
s: β- corpus specific cells in the body responsible for
estradiol; luteum devo of secondary sex characteristics
estrone;
estriol
 -cause autocrine affects to first increase
sensitivity to FSH by increase receptors
and then icnreaseing LH receptos

↑cilia formation and activity of the oviduct

lining

↑contractility of muscular wall

↑proliferation of the endometrium

↑growth and contractility of the

myometrium

↑epithelial proliferation and glucogen

deposition in vagina

-watery secretion of cervical glands

-inhibits osteoclastic activity to promote

bone growth preventing osteoporesis
progester ↑secretion of oviduct lining
one
↓contractility of muscular wall

↑differentiation and secretion of

endometrium

↓contractility of myometrium

↑epithelial differentiation of vagina

↓epithelial proliferation of vagina

-dense, viscous secretion from cervical

glands
hCG Placenta -causes persistent corpus luteum to Peaks
prevent menstruation by continuing to first
(syncytial secrete estrogen and progesterone trimester
trophoblast
cells) -causes endometrium to continue to grow
and store large amounts of nutrients
HCS/HPL Palcenta -partial development of breast and maybe
lactation in animals

-similar to GH but need lots of HPL to

promote growth

-↓ insulin sensitivity and ↓ utilization of

 glucose in mother making more available
for the baby (hyperglycemia)

-promotoes release of FFA from mom to

baby
Oxytocin Posterior Hypothalamus -increases uterine contractions
pituitary
-cervical stretch -causes contraction of mammary gland
receptors alveoli for milk let down
Prolactin Anterior Suckling Dopamine -promotes milk production and secretion
pituitary into alveoli
pregnancy
Testoster Leydig LH -enters cell, 5 alpha reductase converts to -secondary sex characteristics; external Peaks 8
one cells DHT genitalia, pigmentation, facial and body weeks,
hair, prostate, voice, libido, linear growth, one year,
-circulates bound to sex hormone binding epiphyseal fusion and
globulin puberty
-causes transcription
-fetal development of epididymis, vas
-acts on sertoli cells to cause synthesis of deferens, seminal vesicles
androgen binding protein which causes a
local testosterone sink that sucks up huge -pubertal growth of penis, seminal
numbers preventing it from escaping and vesicles, musculature, skeleton, larynx
bathing developing sperm with huge
amounts of T because increasing bound T -spermatogenesis
increases free T so always in equilibrium
DHT -activates transcription -fetal development of penis, penile
urethra, scrotum, prostate

-pubertal growth of scrotum, prostate,

sexual hair sebaceous glands

-prostatic secretion